T cells normally get activated upon stimulation of their T cell receptors (TCR) present on their cell surface. Physiologically this happens when a T cell encounters an antigen presenting cell, like dendritic cells or B cells, displaying major histocompatibility complex (MHC) molecules loaded with antigenic peptide fragments. This in turn results in recruitment and activation of multiple cytosolic proteins such as phospholipase C (PLC), linker for activation of T cells (LAT) and src homology (SH)2 domain-containing leukocyte-specific phosphoprotein of 76 kDa (SLP-76). Activation of PLC leads to the generation of inositol-1,4,5-triphosphate (InsP3) from phosphatidylinositol-4,5-biphosphate (PIP2), in turn binding to InsP3 receptors (InsP3R) in order to trigger Ca2+ release from intracellular endoplasmic reticulum (ER) stores (Gallo et al., Nat. Immunol. 7:25-32, 2006; Lewis et al., Annu. Rev. Immunol. 19:497-521, 2001), which results in an increase in cytosolic calcium levels that is dependent on the presence of coronin 1 (Jayachandran et al., Cell 130:37-50, 2007). Increase in cytosolic calcium results in the activation of calcineurin, which induces translocation of NFAT (nuclear factor of activated T cells) into the nucleus, where it activates genes essential for T cell activation and T cell immune responses (see FIG. 1). Inhibition of the calcineurin pathway results in reduced T cell mediated immune responses. Inhibitors of this pathway are commonly used to treat patients with autoimmune disorders as well as in prevention of immune responses following an organ transplantation that often results in the rejection of transplanted organ. The most widely used are the calcineurin inhibitors cyclosporin A (CsA) and FK506, which form complexes that ultimately inhibit calcineurin function. WO 2007/110385 describes the use of coronin 1 and coronin 1 modulators for the treatment of autoimmune and lymphoproliferative disorders and mycobacterial infections.